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Pica et al. Vessel Plus 2022;6:10  https://dx.doi.org/10.20517/2574-1209.2021.81  Page 9 of 11

               Table 1. The current role of CMR parameters for diagnosis, prognosis, and pathophysiological assessment in cardiac amyloidosis
                                                Diagnosis       Prognosis       Physiopathology
                Morphology and function         +               +               +
                Native T1                       ++              ++              ++
                T2                              -               +               ++
                ECV                             +++ (early)     +++             ++
                LGE                             +++             +++             +



               Tracking changes of the cardiac substrate has the potential to redefine cardiac response to treatment,
               allowing the discrimination of patients with lower risk of progression and patients with the need to intensify
               or change therapy. Furthermore, the ability to measure the amyloid burden could be of value as an endpoint
               in clinical trials for the development of new therapies.

               CONCLUSION
               CMR assessment provides a detailed morpho-functional analysis and a unique tissue characterization of the
               myocardial substrate in CA with prognostic value. Furthermore, CMR quantitative mapping is a promising
               tool for early diagnosis and monitoring of myocardial response to therapies.

               DECLARATIONS
               Authors’ contributions
               Conception, design and writing of the manuscript: Pica S
               Revision the manuscript critically and approval the final manuscript submitted: Lombardi M


               Availability of data and materials
               The data underlying this article will be shared on reasonable request to the corresponding author.

               Financial support and sponsorship
               This study was in part supported by the Ministry of Health, Italy.

               Conflicts of interest
               Both authors report no potential conflicts of interest with Industries or other Institutions that could be
               construed as a conflict of interest related to the present work.


               Ethical approval and consent to participate
               Not applicable.


               Consent for publication
               Not applicable.


               Copyright
               © The Author(s) 2022.


               REFERENCES
               1.       Rapezzi C, Merlini G, Quarta CC, et al. Systemic cardiac amyloidoses: disease profiles and clinical courses of the 3 main types.
                   Circulation 2009;120:1203-12.  DOI  PubMed
               2.       Kyle RA, Linos A, Beard CM, et al. Incidence and natural history of primary systemic amyloidosis in Olmsted County, Minnesota,
                   1950 through 1989. Blood 1992;79:1817-22.  PubMed
               3.       Brenner DA, Jain M, Pimentel DR, et al. Human amyloidogenic light chains directly impair cardiomyocyte function through an
                   increase in cellular oxidant stress. Circ Res 2004;94:1008-10.  DOI  PubMed
               4.       González-López E, Gallego-Delgado M, Guzzo-Merello G, et al. Wild-type transthyretin amyloidosis as a cause of heart failure with
   45   46   47   48   49   50   51   52   53   54   55